Raction in normal rats. In PCP-treated rats, which are characterized by deficient AEA mobilization, endocannabinoid elevation back to handle levels, or direct activation of CB1 receptors or blockade of CCK2 receptors, reverses the social behavior deficit. By contrast, when AEA concentration is elevated above handle levels, as inside the case of saline-treated animals getting URB597, AEA may possibly lose its selective inhibitory action on CCK interneurons and target the cannabinoid-/ vanilloid-sensitive receptor on excitatory terminals (Pistis et al, 2004). A equivalent phenomenon has been reported in the hypothalamus of mice where blockade of AEA reuptake did permit this endocannabinoid to reach glutamatergic inputs (Hentges et al, 2005).Deficient CB1 activation in social withdrawal A Seillier et alIn conclusion, we propose that the negative symptoms of schizophrenia are linked to a deficiency in CB1 receptor function. This observation may possibly reconcile quite a few controversial findings and give a new frame to know the cannabis self-medication hypothesis for damaging symptoms.ACKNOWLEDGEMENTSThis work was supported by NARSAD and NIMH RO1MH91130-01A1 (to AG).DISCLOSUREThe authors declare no conflict of interest.
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